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Pharm Block 11 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

How common are arrhythmias

A

Pretty common
25% of pts treated with digoxin
50% of anesthetized pt
80% pts with acute MI

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2
Q

Do we normally treat arrhymias that are too fast or too slow?

A

Too fast

Tachy arrhythmia

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3
Q

Pros and cons of arryhmias

A

Can be life saving
On the other hand, there is a danger with antiarrhymic drugs in that they can paradoxically precipitate lethal arrhythmia in some patients

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4
Q

Where does the heart beat originate in

A

SA node

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5
Q

How does the beat travel

A

Goes from the SA node down the atria to the AV node

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6
Q

Gate keeper to the ventricles

A

AV

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7
Q

Which is worse, ventricular tachycardia or atrial tachycardia

A

Ventricular

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8
Q

What do we want to target when we treat atria?

A

AV node

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9
Q

What is the path of heart conduction

A

SA node, down atria, to AV node, purkinje, to ventricular

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10
Q

What does every step of conduction create?

A

AP

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11
Q

SA node AP

A

Hill

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12
Q

Atrial muscle AP

A

Steep AP

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13
Q

AV node AP

A

Hill

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14
Q

Perkinje AP

A

Steep

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15
Q

Ventricular muscle AP

A

Steep

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16
Q

Where do meds work for arrhythmia

A

On muscles and perkinje because of the steep AP

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17
Q

P waves

A

Atria gets excited

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18
Q

PR interval

A

Atrial conduction

SA node down to the AV node, span of atrial excitation

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19
Q

QRS interval

A

Ventricular being excited

Ventricular depolarization start

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20
Q

T wave

A

Ventricles repolarization

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21
Q

QT intervals

A
  • ventricular depolarization to repolarization

- represents entire ventricular conduction

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22
Q

Fast response AP

A

Heart and Perkinje

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23
Q

Fast response in phase 0

A

Happen quickly, steep

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24
Q

What drugs do we use for fast response AP arrhymias?

A

Na channel blockers

K channel blockers

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25
Q

Na channel blockers in fast response AP arrhythmias

A

Depolarization causes by influx of Na, Na starts this AP and causes phase 0
-blockers with cause shift to right and less steep, means it takes longer to depolarize, slowing heart down

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26
Q

K channel blockers in fast response AP arrhymias

A
  • K repolarizes membrane
  • increased K inside the cell, rushing out to repolarize
  • longer to repolarize with these blockers
  • AP gets wider, took more time, slowed the heart down
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27
Q

Where is the most muscle in the heart

A

Ventricles

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28
Q

What drugs work on the ventricles

A

Na channel and K channel blockers

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29
Q

What doe Na and K channel blockers do on the ventricles

A

Depress ventricular depolarization

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30
Q

Na channel blockers affects what interval

A

Longer QRS interval

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31
Q

What interval do K channel blockers affect

A

Increased QT interval

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32
Q

What type of drugs treat ventricular arryhmias

A

K and Na channel blockers

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33
Q

Slow response AP

A

Gradaul and not as steep

AV and SA node

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34
Q

Phase IV in slow response

A

Spontaneous depolarization

-in ventricles it is flat.

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35
Q

Why is the SA node the pacemaker?

A

Because it is the only place in the heart with a phase IV that is as steep as it is.
-it is flat in ventricles

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36
Q

Where are the funny Na channels

A

Slow response AP
AV and SA
Phase IV

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37
Q

Phase 0 in slow phase

A

All Ca channels

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38
Q

What drugs do we use to treat slow response AP (SA and AV nodes)

A

Ca2+ channel blocker

B blockers

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39
Q

Ca2+ channel blockers used for slow response AP in arrhythmias

A
  • Blocks 0 phase
  • in fast response this would be Na
  • depress phase IV and 0
  • slow heart at SA and AV node
  • if you are slowing the conduction from SA to AV, then you are slowing the atrial conduction
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40
Q

What drugs slows the PR interval?

A

Ca2+ channel blockers

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41
Q

B blockers in treating slow response AP for arrhythmias

A
  • dobutamine
  • if you block B receptors, you are decrease cAMP, decreasing PKA, not phosphorylation Ca2+ channels so they wont open
  • indirectly blocks Ca2+
  • decreased Ca2+
  • depresses phase IV and 0
  • good for nodes (B1 concentrated in the nodes)
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42
Q

What does altering calcium do to the AP?

A

Depresses phase IV and 0 in slow response AP

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43
Q

What do we use B blockers and Ca2+ channel blockers for?

A

Used to treat SVT (supraventricular tachycardia)
-does this by slowing the conduction between the SA and AV node, which ultimately slows atrial conduction
-

44
Q

What kinds of meds are used to treat ventricular arrhymias

A

Na blockers

K blockers

45
Q

What kind of drugs are used to treat SVT (supraventricular tachycardia/atrial)

A

Ca2+ blocker

B blocker

46
Q

Types of SVTs

A

Atrial fibrillation

Paroxysmal SVT

47
Q

Which is more life threatening: ventricular or atrial arrhythmias

A

Ventricular

48
Q

What is the most common arrhythmia

A

Afib

49
Q

Why is it important to treat SVTs even though they are not as dangerous as ventricular arrhythmia s

A

You need to control the AV node for SVT so that it does not make its way into the ventricles.

50
Q

Types of ventricular arrhythmias

A
  • premature ventricular complexes (PVCs)
  • ventricular tachycardia
  • ventricular fibrillation
51
Q

Premature ventricular complexes (PVCs)

A

Non-life threatening. Most people experience these, can lead to ventricular tachycardia

52
Q

Ventricular tachycardia

A
  • three or more repetitive PVCs cause this
  • monomorphic
  • polymorphic
  • leads to V fib if uncontrolled
53
Q

Ventricular fibrillation

A
  • electrical anarchy

- death ensues rapidly without tx

54
Q

Monomorphic Vtach

A

Consistent QRS configuration

55
Q

Polymorphic V-tach

A

Varying QRS complexes

-torsade de pointes where the QRS complexes undulate around a central axis, baseline moves all over the place

56
Q

Torsades

A
  • Type of polymorphic V tach

- QRS complex undulates around a central axis

57
Q

How are the antiarrhymic drugs categorized

A

Class I-IV

Saved By Pharm Class

58
Q

Class I antiarrhythmic drugs

A
  • sodium channel blockers

- class 1A, 1B, and 1C

59
Q

Class II antiarrhythmic drugs

A

-B blockers

60
Q

Class III antiarrhythmic drugs

A

K channel blockers

61
Q

Class IV antiarrhythmic drugs

A

Calcium channel blockers

62
Q

Class IA antiarrhythmic drug

A

-quinidine

63
Q

Class IA antiarrhythmic drug (quinidine) cardiac effects

A

Block Na channels and K channels; can cause widening of the QRS and QT intervals; also has antimuscarinic and a1 blocking effects to increase HR and can further cause arrhythmias

64
Q

Class 1A antiarrhythmic drugs (quinidine) therapeutic use

A

Prevent recurring v tach

May increase mortality

65
Q

Adverse effects of class 1A antiarrhythmics (quinidine)

A

Potential example torsades de pointes due to K channel block

  • prolonged repolarization for too long, ventricles have their own intrinsic firing rate if they wait too long
  • torsade is caused no K channel blockers, even though class IA is Na channel blocker, it does have some K channel blocking properties
66
Q

What does blocking Na channels with a class 1A antiarrhythmic drug do

A

Prolongs ventricular depolariation

67
Q

What does blocking of K channels with a class 1A antiarrhthymic drug do

A

Prolongs ventricular repolarization

68
Q

What class of antiarrhymics can lead to torsades?

A 
All class 1A 
Class III
69
Q

Class 1B antiarrhymic drug

A

Lidocaine

70
Q

Cardiac effects of class 1B antiarrhymic drugs (lidocaine)

A

Dosing channel blocker only

71
Q

Therapeutic use of class 1B antiarrhymic drugs (lidocaine)

A

Ventricular arrhythmias

72
Q

How are class 1B antiarrhythmics administered (lidocaine)

A

IV due to extensive first pass metabolism

73
Q

When do we use class 1B antiarrhymics?

A

Only in acute settings

74
Q

Class 1C antiarrhymic drug

A

Flecainaide

75
Q

Cardiac actions of class Ic antiarrhymic drugs (flecainaide)

A

Blocks sodium

76
Q

Therapeutic uses of class 1C antiaarhymic drugs

A

Prevent a fib, increased mortality in patients with ventricular arrhymias

77
Q

When do we want to use class I drugs

A

Back up only

All kinda scary

78
Q

What are the specific class II antiarrhythmics drugs

A

Atenolol and metoprolol

79
Q

Class II antiarrhythmics

A

B blockers

  • diminish phase IV and 0 depolarization
  • depress automaticity at the SA node, prolong AV conduction, decrease HR
  • PR interval prolonged
  • good for SVTs (atrial)
80
Q

What drugs are best for SVT

A

Class II antiarrhythmics (B blockers)

81
Q

Class III antiarrhymics

A

Potassium channel blockers

82
Q

What is the specific drugs for class III antiarrhymics

A

Sotalol
Amiodarone
Dronedarone

83
Q

Cardiac actions of sotalol (class III antiarrthymics)

A

Block K channels and B receptors

  • K channels for ventricular
  • B receptors for SVT
84
Q

Therapeutic use of sotalol (class III antiarrhymic drugs)

A

Ventricular arrhythmia and SVTs

85
Q

Adverse effects of sotalol (class III antiarrhymics)

A

Bradycardia, dyspnea, fatigue (all related to B blockade); torsades (bc of K blockade)

86
Q

What’s the difference between amiodarone and dronedarone

A

Dronedarone does not contain iodine

87
Q

Actions of amiodarone/dronedarone (class III antiarrhythmics)

A 
Amiodarone contains iodine and is related to thyroxin; both drugs similar to class I, II, III, and IV
-prolongs PR, QRS, and QT
88
Q

Therapeutic uses of amiodarone and dronedarone (class III antoarrhythmics)

A

Multipurpose

89
Q

Half life of amiodarone

A

Several weeks

90
Q

Half life of dronedarone

A

24 hours

91
Q

Adverse effects of amiodarone and dronedarone

A

Pulmonary alveolitis or fibrosis, hpatotoxicity, corneal deposits, thyroid dysfunction and blue skin (amiodarone)

92
Q

What drug can produce lung, liver, and eye problems?

A

Amiodarone and dronedarone

93
Q

Which drug can cause thyroid problems and blue skin

A

Amiodarone

94
Q

Pt is started on an antiarrhythmic drug that blocks Na, K, B, and Ca. Patient complains of bluish skin, what drug could this be

A

Amiodarone

95
Q

Class IV antiarrhythmic

A

Ca2_ channel blocker

96
Q

What do class IV antiarrhythmic drugs do

A

Decrease rate of phase IV and 0

Slowed conduction in SA, AV

97
Q

What are the specific class IV antiarrhythmic drugs

A

Verapamil and diltiazem

-used for SVT

98
Q

Can amlodipine be a good choice of CCB to use for arrhythmias?

A

No, we only want the ones that work on the heart. Amlodipine only works on the vessels

99
Q

What are the unclassified antiarrhythmic drugs

A

Digoxin

Adenosine

100
Q

What can digoxin be used for

A

Heart failure and arrhythmias

  • increase contractility for HF
  • slows HR by increasing vagaries firing for arrhythmias
101
Q

Cardiac action of digoxin in arryhthmias

A

PNS effects on the atria and AV node; it can increase the PR interval due to slowing conduction in the AV node
-increased PNS activation by increased Vargas firing)

102
Q

Therapeutic use of digoxin

A

SVT

103
Q

Actions of adenosine

A

Naturally occurring nucleoside, decreases conduction velocity by working on adenosine receptors in the heart (Gi)

104
Q

Therapeutic use of adenosine

A

Drug of choice for abolishing acute SVT

105
Q

How must adenosine be administered

A

IV, acute only

Only has a duration of action of about 8s

106
Q

What happens when you use adenosine on a patient

A

Causes them to temporarily flat line, resets the heart back to sinus rhythm

Pharm Block 11 (7 decks)

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